Reply to "Human neural progenitor cells: better blue than green?"
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Journal Article↗
Biomedical subjects
N Roy
Publications and source records attributed to N Roy.
Personality traits and psychological factors in voice pathology: a foundation for future research.
It has been argued that personality, emotions, and psychological problems contribute to or are primary causes of voice disorders and that voice disorders in turn create psychological problems and personality effects. This article (a) briefly reviews the literature surrounding the role of psychological and personality processes in individuals with functional dysphonia (FD), vocal nodules (VN), and spasmodic dysphonia (SD); (b) provides an overview of recent concepts in personality and trait structure; and (c) summarizes the fundamental tenets of a theoretical synthesis proposed by Roy and Bless (2000) to explain the dispositional bases of FD and VN. This theory links FD and VN to the signal sensitivities and behavioral response biases of neurotic introverts and neurotic extraverts, respectively. In a companion article, the merits of the Roy and Bless theory are evaluated.
Humans↗
Personality and voice disorders: a superfactor trait analysis.
To determine whether personality factors play causal, concomitant, or consequential roles in common voice disorders, a vocally normal control group and four groups with voice disorders-functional dysphonia (FD), vocal nodules (VN), spasmodic dysphonia (SD), and unilateral vocal fold paralysis (UVFP)-were compared on measures of personality and psychological adjustment. Superfactor group comparisons revealed that the majority of FD and VN subjects were classified as introverts and extraverts, respectively. Comparisons involving the SD, UVFP, and control subjects did not identify consistent personality differences. The disability hypothesis, which suggests that personality features and emotional maladjustment are solely a negative consequence of vocal disability, was not supported. Personality variables and their behavioral consequences may therefore contribute to FD and VN. Results are presented within the context of a dispositional theory offered by Roy and Bless (2000a).
Adult↗
Purification and some properties of high-molecular-weight xylanases, the xylanases 4 and 5 of Aeromonas caviae W-61.
Aeromonas caviae W-61 produces multiple extracellular xylanases, the xylanases 1, 2, 3, 4, and 5 [Nguyen, V. D. et al., Biosci. Biotechnol. Biochem., 56, 1708-1712 (1993)]. Here we purified and characterized high-molecular-weight xylanases, the xylanases 4 and 5 from the culture fluids of the bacterium. The purified xylanases 4 and 5, which had molecular masses of 120 and 140 kDa, respectively, were endo-beta-1,4-xylanases with similar enzymatic properties except for trans-xylosidase activity. The xylanase 4 showed a prominent transxylosidase activity when xylotriose and xylotetraose were used as the substrates, while the xylanase 5 had little transxylosidase activity under the same conditions. Protein sequencing indicated that the xylanase 4 was a C-terminally-truncated xylanase 5, suggesting that the C-terminal truncation of the xylanase 5 may endow the enzyme with transxylosidase activity.
Aeromonas↗
The distinct HERG missense mutation L564P causes long QT syndrome in one French Canadian family.
BACKGROUND: Long QT syndrome is a congenital abnormality of cardiac repolarization causing syncope and sudden death from ventricular tachyarrhythmias known as torsades de pointes. This hereditary cardiac disorder often shows an increase of the value of the QT interval corrected for heart rate over 0.45 s in a 12-lead electrocardiogram. OBJECTIVE: To find and identify pertinent mutations occurring in French Canadians by extracting genomic DNA from blood samples and performing a combination of polymerase chain reaction (PCR), single-strand conformational polymorphism and DNA sequencing. RESULTS: A novel mutation was identified in the S5 region of the HERG potassium channel. In codon 564 CTA, T was replaced by C, resulting in a leucine to proline substitution. Two family members had the mutation in two distinct generations. A new restriction site was created at this position and therefore enabled the development of a rapid diagnostic test using PCR. HERG wild type and mutant potassium channel mRNAs were then expressed in Xenopus laevis oocytes. CONCLUSION: This electrophysiological study suggests that coexpression of HERG wild type and mutant L564P results in a dominant negative effect of the mutation.
Adult↗
Chemical and immunochemical studies of the O-antigen from enteropathogenic Escherichia coli O158 lipopolysaccharide.
The O-specific polysaccharide isolated from Escherichia coli O158 smooth lipopolysaccharide contains L-rhamnose, D-glucose and 2-acetamido-2-deoxy-D-galactose in the molar ratios 1:2:2. Studies on composition, methylation analysis and specific degradations together with a 1H and 13C NMR spectral study established that the O-antigen is built up from a pentasaccharide repeating unit having the following structure: [formula: see text] The most effective inhibitory part of the oligosaccharide from E. coli O158 lipopolysaccharide has been serologically characterized by an ELISA-inhibition study using different sugars. The results showed that methyl alpha- and beta-D-GalpNAc are the most effective inhibitors among the monosaccharides tested, while the main antibody specificity lies on the main-chain trisaccharide repeating unit.
Carbohydrate Sequence↗
Comparison of propafenone versus procainamide for the acute treatment of atrial fibrillation after cardiac surgery.
A prospective, randomized, double-blind study to compare the efficacy in terminating postoperative atrial fibrillation of the class Ic drug propafenone versus class Ia drug procainamide was conducted. Intravenous propafenone was superior to procainamide in achieving rapid cardioversion and a better rate control with a lower incidence of symptomatic hypotension.
Aged↗
Expression of human gelatinase B in Pichia pastoris.
Full-length human gelatinase B (FLGelB) and its C-terminal truncated form (dGelB) were expressed in Pichia pastoris strain GS115, using the Saccharomyces cerevisiae Mat alpha signal peptide. In both cases, a high level of the secreted protein could be detected by SDS-PAGE. The truncated gene was also expressed using the human gelatinase B native signal peptide. Secretion using the Mat alpha signal peptide was significantly greater than that from the native signal peptide. The recombinant products were purified and characterized biochemically. The recombinant proteins, FLGelB and dGelB, were found to have similar biochemical properties and activity to that of the human gelatinase B native protein.
Base Sequence↗
The ZDS1 and ZDS2 proteins require the Sir3p component of yeast silent chromatin to enhance the stability of short linear centromeric plasmids.
Yeast artificial chromosome (YAC) clones of Saccharomyces cerevisiae containing a centromere, origin of replication, two telomeres and a >50 kb insert of DNA are maintained as normal yeast chromosomes. However, short linear centromeric plasmids of 10-15 kb in size (short YACs) are missegregated at a much higher frequency than long YACs or 10-15 kb circular centromeric plasmids. A search for genes that stabilized short linear centromeric plasmids when present in multiple copies per cell uncovered ZDS1, which reduced the rate at which cells lost the short YAC, increased the fraction of cells that maintained the short YAC and decreased the number of short YACs per cell. Multiple copies of ZDS2, a homolog of ZDS1, had similar effects. Genes near yeast telomeres are transcriptionally silenced by the recruitment of proteins encoded by the SIR2, SIR3 and SIR4 genes (Sir2p, Sir3p and Sir4p). Multiple copies of ZDS1 and ZDS2 caused an increase in telomeric silencing. In addition, ZDS1 and ZDS2 both required the open reading frame encoding the N-terminal 174 amino acids of Sir3p to stabilize short YACs. Thus, the short YAC stability assay revealed a silencing-independent function for the Sir3p N-terminus. Two-hybrid analysis indicated that Zds1p and Zds2p interact with Sir2p, Sir3p, Sir4p or the yeast telomere binding protein Rap1p. Deletion of both ZDS1 and ZDS2 made short YACs, but not a 100 kb YAC, extremely unstable and also caused a 70 bp increase in the length of the telomeric TG1-3 repeats. These data indicate that short YACs can be stabilized by trans-acting factors and suggest that the proteins encoded by ZDS1 and ZDS2 alter short YAC stability by interacting with proteins that function at the telomere.
Adaptor Proteins, Signal Transducing↗
Self-organizing map for the classification of normal and disordered female voices.
The goal of this research was to train a self-organizing map (SOM) on various acoustic measures (amplitude perturbation quotient, degree of voice breaks, rahmonic amplitude, soft phonation index, standard deviation of the fundamental frequency, and peak amplitude variation) of the sustained vowel /a/ to enhance visualization of the multidimensional nonlinear regularities inherent in the input data space. The SOM was trained using 30 spasmodic dysphonia exemplars, 30 pretreatment functional dysphonia exemplars, 30 post-treatment functional dysphonia exemplars, and 30 normal voice exemplars. After training, the classification performance of the SOM was evaluated. The results indicated that the SOM had better classification performance than that of a stepwise discriminant analysis over the original data. Analysis of the weight values across the SOM, by means of stepwise discriminant analysis, revealed the relative importance of the acoustic measures in classification of the various groups. The SOM provided both an easy way to visualize multidimensional data, and enhanced statistical predictability at distinguishing between the various groups (over that conducted on the original data set). We regard the results of this study as a promising initial step into the use of SOMs with multiple acoustic measures to assess phonatory function.
Adult↗
MCM21 and MCM22, two novel genes of the yeast Saccharomyces cerevisiae are required for chromosome transmission.
The minichromosome maintenance genes, MCM21 and MCM22, have been cloned and are shown to code for the ORFs YDR318W and YJR135C respectively. Mutations in these genes caused a decrease in the stability of the minichromosome. This decrease in stability was associated with an increase in the copy number of the minichromosome in cells carrying it. Small circular dicentric plasmids were maintained relatively stably and structurally intact in the mutants compared with the wild-type strain. In the latter, such plasmids were mitotically unstable and, upon recovery, showed frequent rearrangements of their DNA. A centromere offered less obstruction to transcription in mutant cells than in the wild type, showing that both these mutants had a more relaxed kinetochore assembly. The mutant strains showed elevated rates of chromosome loss but not those of recombination. Both the mutations caused the cells to display a higher sensitivity towards the anti-mitotic drug benomyl. All these observations suggest that MCM21 and MCM22 are important for chromosome segregation with a potential role in kinetochore function. These genes are non-essential, as their deletions from chromosomes did not cause loss of cell viability. However, exponentially growing mutant cells carrying the deletion of the MCM21 gene had a significant population of large-budded cells with a single nucleus at the neck. Furthermore, the DNA content of these cells showed a shift towards 2N, suggesting a temporary pause of cells in G2 or in an early phase of mitosis. The mcm21 and mcm22 mutations do not show synthetic lethality or any further enhancement of growth defects, implying that they could be carrying out non-overlapping functions in chromosome segregation.
Cell Cycle Proteins↗
Laparoscopic resection does not adversely affect early survival curves in patients undergoing surgery for colorectal adenocarcinoma.
OBJECTIVE: To determine the survival curves for laparoscopic resection (LR) of colorectal cancer. SUMMARY BACKGROUND DATA: Laparoscopic resection for cure of colorectal cancer is controversial, and survival curves have not been determined. METHODS: A prospective database of 177 consecutive LRs of colorectal cancers performed between November 1991 and 1997 was reviewed. The TNM classification (stage 0, I, II, III, and IV) for colorectal cancers and the Kaplan-Meier method were used to determine survival curves. RESULTS: Of the 177 patients, 5 were excluded for not having adenocarcinomas. Twenty-five patients (14.5%) had conversion to open surgery; most of these patients had rectal cancer or tumor invasion to adjacent organs. Twelve patients were lost to follow-up. All 135 remaining patients had follow-up. Overall, 28 deaths occurred during the follow-up period, 15 of which were cancer-related. The median follow-up was 24 months for patients with stage I, II, and III disease and 9 months for patients with stage IV disease. Observed 2-year survival rates were 100% stage I, 88.7% stage II, 80.6% stage III, and 28.6% stage IV. Survival rates at 4 years were 100% stage I, 79.5% stage II, 53.7% stage III, and 0% stage IV. No trocar site recurrence was observed. CONCLUSIONS: Early survival curves for patients with colorectal cancer who underwent LR do not differ negatively from historical controls for conventional surgery. Further validation is needed.
Adenocarcinoma↗
Regulation of cell death protease caspase-9 by phosphorylation.
Caspases are intracellular proteases that function as initiators and effectors of apoptosis. The kinase Akt and p21-Ras, an Akt activator, induced phosphorylation of pro-caspase-9 (pro-Casp9) in cells. Cytochrome c-induced proteolytic processing of pro-Casp9 was defective in cytosolic extracts from cells expressing either active Ras or Akt. Akt phosphorylated recombinant Casp9 in vitro on serine-196 and inhibited its protease activity. Mutant pro-Casp9(Ser196Ala) was resistant to Akt-mediated phosphorylation and inhibition in vitro and in cells, resulting in Akt-resistant induction of apoptosis. Thus, caspases can be directly regulated by protein phosphorylation.
Apoptosis↗
IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases.
Inhibitor of apoptosis (IAP) gene products play an evolutionarily conserved role in regulating programmed cell death in diverse species ranging from insects to humans. Human XIAP, cIAP1 and cIAP2 are direct inhibitors of at least two members of the caspase family of cell death proteases: caspase-3 and caspase-7. Here we compared the mechanism by which IAPs interfere with activation of caspase-3 and other effector caspases in cytosolic extracts where caspase activation was initiated by caspase-8, a proximal protease activated by ligation of TNF-family receptors, or by cytochrome c, which is released from mitochondria into the cytosol during apoptosis. These studies demonstrate that XIAP, cIAP1 and cIAP2 can prevent the proteolytic processing of pro-caspases -3, -6 and -7 by blocking the cytochrome c-induced activation of pro-caspase-9. In contrast, these IAP family proteins did not prevent caspase-8-induced proteolytic activation of pro-caspase-3; however, they subsequently inhibited active caspase-3 directly, thus blocking downstream apoptotic events such as further activation of caspases. These findings demonstrate that IAPs can suppress different apoptotic pathways by inhibiting distinct caspases and identify pro-caspase-9 as a new target for IAP-mediated inhibition of apoptosis.
Apoptosis↗
Regulation of macrophage phagocytosis of apoptotic cells by cAMP.
Regulation of macrophage capacity to remove apoptotic cells may control the balance of apoptotic and necrotic leukocytes at inflamed foci and the extent of leukocyte-mediated tissue damage. Although the molecules involved in the phagocytic process are beginning to be defined, little is known about the underlying regulatory and signaling mechanisms controlling this process. In this paper, we have investigated the effects of treatment of human monocyte-derived macrophages with PGs and other agents that elevate intracellular cAMP on phagocytosis. PGE2 and PGD2 specifically reduced the proportion of macrophages that phagocytosed apoptotic cells. Similar results were obtained with the membrane-permeable cAMP analogues dibutyryl-cAMP and 8-bromo-cAMP but not with the cGMP analogue dibutyryl-GMP. Consistent with the observation that phagocytosis was inhibited by cAMP elevation, treatment of monocyte-derived macrophages with PGE2 resulted in rapid, transient increase in levels of intracellular cAMP. These effects were not due to nonspecific inhibition of monocyte-derived macrophage phagocytosis given that ingestion of Ig-opsonized erythrocytes was unaffected. Elevation of cAMP induced morphologic alterations indicative of changes in the adhesive status of the macrophage, including cell rounding and disassembly of structures that represent points of contact with substrate containing actin and talin. These results strongly suggest that rapid activation of cAMP signaling pathways by inflammatory mediators regulates processes that limit tissue injury and that modulation of cAMP levels represents an additional therapeutic target in the control of resolution of inflammation.
Apoptosis↗
Cloning, expression, purification, and immunocharacterization of placental protein-14.
Human placental protein-14 (PP-14), a member of the lipocalin superfamily, shares homology at the level of the primary and secondary structures with bovine beta-lactoglobulin. It is the most prominent endometrial protein synthesized by the glandular cells of endometrium under estrogen priming and progesterone stimulation. The temporal and spatial expression of PP-14 in the female reproductive tract combined with its biological activities ex vivo suggest that this glycoprotein probably plays an essential physiological role in the regulation of fertilization, implantation, and maintenance of pregnancy. We proposed to elucidate the molecular mechanisms involved in the function of this protein. A prerequisite to such investigations on any protein is the availability of sufficient amounts of the same in a homogenous form. Therefore, recombinant DNA technology was employed. The PP-14 cDNA was obtained from the first-trimester endometrial tissue RNA by RT-PCR using unique primers. After confirming the identity of the gene, the protein was expressed in Escherichia coli and purified to homogeneity. The gene was also cloned and expressed in Pichia pastoris to obtain the protein product in a glycosylated form. The recombinant proteins were immunocharacterized using a cross-reactive antibody raised to bovine beta-lactoglobulin. Polyclonal antiserum raised to the E coli expressed PP-14 also bound to the native PP-14 from amniotic fluid suggesting that recombinant PP-14 may be exploited to elucidate functional aspects of the protein.
Amino Acid Sequence↗
Synthesis of the tetrasaccharide repeating unit of the K-antigen from Klebsiella type 57.
Starting from D-galactose and D-mannose two disaccharide blocks, namely 2-(trimethylsilyl)-ethyl 2,3,4,6-tetra-O-benzyl-alpha-D-mannopyranosyl-(1-->4)-6-O-(4-methoxybenz yl)- beta-D-galactopyranoside and ethyl 2,3,4,6-tetra-O-benzyl-alpha-D-mannopyranosyl-(1-->3)-4-O-acetyl- 2,6-di-O-benzoyl-1-thio-beta-D-galactopyranoside, were synthesized which were then allowed to react, in the presence of dimethyl(methylthio)sulfonium triflate to give a tetrasaccharide derivative. This compound was converted to 2-(trimethylsilyl)ethyl 2,3,4,6-tetra-O-benzyl-alpha-D- mannopyranosyl-(1-->3)-4-O-acetyl-2,6-di-O-benzoyl-beta-D-galactopyranos yl- (1-->3)-[2,3,4,6-tetra-O-benzyl-alpha-D-mannopyranosyl-(1-->4)]-tert-but yl (2-O-acetyl-beta-D-galactopyranosid)uronate which, on treatment with sodium methoxide followed by hydrogenolysis, afforded the methyl [2-(trimethylsilyl)ethyl glycosid]uronate of the tetrasaccharide repeating unit of the K-antigen from Klebsiella type 57.
Antigens, Bacterial↗
Superior dislocation of the superior tibiofibular joint associated with fracture of the tibial shaft.
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Arthrography↗